The formation of the embryonic palate depends on the movement of the palatine shelves from a vertical to horizontal position above the tongue. To determine whether the movement of the palatine shelves is related to the extension of the cranial base, from which the shelves hang, it is first necessary to correlate changes in morphology of the cranial base with stages of palatine shelf movement. Two strains of mice (A/J and C57B1/6) have different susceptibilities to 6-aminonicotinamide (6 AN) induced cleft palate. The same dose of 6AN injected i.p. on day 13 of gestation produces cleft palate in 100% of the A/J offspring, but only among 65% of the C57B1/6 fetuses. A previous study by this investigator indicated an interruption of development of the cranial base at this time. A comparison of morphogenesis within these two strains will yield information to distinguish whether the concurrent morphogenetic events of cranial base straightening and of transposition of the palatine shelves are causally related. There is one area of very rapid growth in the anterior portion of the cranial base. To determine how this area normally expands and how it is affected by 6AN, it is necessary to determine whether there is increased cell proliferation (by H3 thymidine uptake) or an increase in sulfated mucopolysaccharide intercellular material (by S35 sulfate uptake). This can be visualized by injecting either of these isotopes in the mother before the fetuses are collected, and preparing autoradiographs of mid-sagittal sections of the fetal mouse heads on days 14.5 or 15 of gestation. In this critical period between the injection of 6AN (day 13) and the failure of closure of the palate (days 14.5-15) there is abnormal development of the cranial base. In trying to correlate the teratogenic effects of 6AN in these developmental areas, the early effects of 6AN on the cranial base will be examined by autoradiography at 6, 12, 24, and 36 hours after injection and the data from both strains will be compared.